Published online before print June 9, 2003, doi: 10.1161/01.HYP.0000078829.02288.98
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(Hypertension. 2003;42:61.)
© 2003 American Heart Association, Inc.
Scientific Contribution |
Middle Age Cardiovascular Risk Factors and Abdominal Aortic Aneurysm in Older Age
From the Division of Geriatrics, Department of Medicine, University of Chicago Pritzker School of Medicine (M.B.R.), Chicago; the Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University (M.L.D., K.L., D.B.G., P.G., J.S.), Chicago, Illinois; and the Department of Medicine, St. Mary’s Medical Center (G.C.W.), San Francisco, California.
Correspondence to Jeremiah Stamler, MD, Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, 680 N Lake Shore Drive, Suite 1102, Chicago, IL 60611. E-mail hwe216{at}northwestern.edu
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Abstract |
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Few prospective studies have examined associations between major cardiovascular risk factors and occurrence of abdominal aortic aneurysm; findings from cross-sectional studies are inconsistent. This long-term population-based study assessed relationships of major risk factors in middle-age to clinical nonfatal plus fatal abdominal aortic aneurysm in older-age in the Chicago Heart Association Detection Project in Industry cohort—10 574 men and 8700 women baseline ages 40 to 64 years screened for risk factors in 1967–1973 at workplaces. With average follow-up of 30 years and clinical cases identified from Medicare records and death certificates, risk factor relationships to abdominal aortic aneurysm occurrence were assessed by Cox regression. There were among men 309 cases and among women, 109—most from Medicare records. Most findings were qualitatively similar for men and women. In multivariate analyses (5 models), hazard ratios for abdominal aortic aneurysm were significantly greater for men than women (
1.97), with older age ( BORDER="0">1.63/5 years), higher serum cholesterol (1.30/40.0 mg/dL), cigarettes/d (2.43/20 cigarettes), past smoking (1.41), height (1.17/7 cm), evidence of adverse blood pressure (hazard ratio 1.10/20 mm Hg higher systolic pressure, 1.12 to 1.14/12 mm Hg higher diastolic pressure, 1.87 with history of treated hypertension). It is concluded that major cardiovascular risk factors—serum cholesterol, smoking, and blood pressure—in middle age relate significantly to risk of abdominal aortic aneurysm in persons surviving into older age.
Key Words: abdominal aortic aneurysm • risk factors • prospective studies • blood pressure • cholesterol • smoking
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Introduction |
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Clinical aortic aneurysm is an important cardiovascular disease in older people. Preclinical aneurysm development is insidious; co-morbidity complicates treatment of aneurysm whether it is discovered incidentally, by deliberate screening, or following an acute rupture.1 Therefore prevention of this condition, via risk factor identification and treatment, is a pertinent clinical issue for older population strata. Much of the understanding of possibly modifiable risk for this disease of later life is derived from cross-sectional screening surveys and clinical series.2–11 These studies have typically shown associations of such cardiovascular disease (CVD) risk factors as male gender, older age, and smoking with prevalent abdominal aortic aneurysm (AAA) and aneurysm progression.2–11 Findings have been inconsistent, however, for hypertension,6,9,12 serum cholesterol,3,6,8,10 diabetes,3,4,9 and such other possible risk factors as body habitus3,9,13 and race.3,4
There are relatively few prospective population studies on relationships of CVD risk factors to AAA, and these have been limited by paucity of risk factor data, short duration of follow-up, small number of cases leading to inclusion of all types of aortic aneurysms regardless of site.14–19 This report is from a long-term large population-based study on relationships of major modifiable CVD risk factors, measured in middle-aged employed persons, to CVD incidence and mortality in later life. It assesses prospectively relationships of risk factors to clinically identified nonfatal plus fatal AAA.
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Methods |
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Study Population
The Chicago Heart Association (CHA) cohort consists of nearly 40 000 employed men and women screened for major cardiovascular risk factors from late 1967 to early 1973 at 84 work sites. Potential risk factors were determined by self-administered questionnaire for age, ethnicity, education, cigarette smoking, history of coronary heart disease (CHD), diagnosed diabetes, and high blood pressure. Standardized procedures were used to obtain height, weight, a single supine blood pressure, and a resting ECG. Major and minor ECG abnormalities were coded by Pooling Project criteria.20 Blood was drawn to determine serum cholesterol and plasma glucose, measured 1 hour after a nonfasting 50-g oral glucose load. Participant recruitment and examination protocols have been described.21
This analysis is based on 10 661 men and 8817 women, ages 40 to 64 at baseline, who could have reached at least age 65 in the year 2000. After exclusion of participants with incomplete baseline data, 10 574 men and 8700 women remained for analysis. Participants were excluded for missing values as follows: n=87 cholesterol, n=12 blood pressure, n=6 BMI, n=47 education, n=8 smoking, and n=44 diabetes history. As reported, the time interval for blood drawing affected blood glucose values.22 Therefore, in analyses on plasma glucose and AAA, 1000 women and 1031 men were excluded from whom blood had been taken without a recorded time or for whom more than 65 minutes had passed between oral glucose load and blood drawing.
Follow-Up and Case Ascertainment
Follow-up averaged 30 years. For the entire cohort, the National Death Index was searched periodically for vital status. For all decedents through 1992, death certificates were obtained from states and coded for up to 5 causes of death according to the International Classification of Diseases, 8th Revision (ICD-8).23 For all decedents between 1993 and 2000, information was obtained from the National Death Index–Plus (NDI). NDI provided up to 15 causes of death coded according to the 9th (ICD-9) and 10th (ICD-10) revisions of the International Classification of Diseases.22–24 Health Care Financing Administration (HCFA) tapes for Medicare Part A (inpatient) and Part B (outpatient) were obtained for eligible participants for the years 1984–2000. The tapes contain a record of each Medicare reimbursable medical encounter, including date of service and between 5 and 9 billing codes, based on the International Classification of Diseases, 9th Revision (ICD-9).24 AAA was defined as the first chronological occurrence of any mention of ICD-8 code 441.2, ICD-9 codes 441.3 or 441.4, or ICD-10 codes 171.3 or 171.4 on a death certificate, NDI record, or a Medicare billing record.25,26 Death certificates, NDI, and Medicare encounter records were searched for other CVD, including coronary, peripheral arterial, and cerebrovascular diseases, and for diagnoses of diabetes and chronic obstructive pulmonary disease (COPD). COPD was included because of its association with smoking and its putative association with a generalized defect in collagen-elastin synthesis.27
Statistical Analyses
Crude and age-adjusted rates of AAA were computed per 10 000 person-years of follow-up for each gender separately. Persons with AAA were compared with all other participants for baseline characteristics including age, education, race, serum total cholesterol, current or past smoking, cigarettes smoked per day by current smokers, systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure, The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VI) BP stratification,28 history of treated hypertension, major and minor ECG abnormalities, height, weight, body mass index (BMI, in kg/m2), history of diabetes, and 1-hour post-load plasma glucose for nondiabetics. To assess relationships of baseline variables to occurrence of AAA, both continuous and categoric analyses were done. For example, in categoric analyses serum cholesterol was stratified <200, 200 to 239, 240 mg/dL. In continuous analyses, age- and multivariate-adjusted relative risks were first computed for each gender separately using Cox multivariate proportional hazards models.29 The Schoenfeld residuals method was used to assess whether continuous data met the assumption of proportional hazards.30 In final Cox multivariate models, the impact of major risk factors considered together—with each adjusted for all others—was assessed for men and women combined, with control for gender. Several multivariate models were computed, to assess separately the independent relationship of each blood pressure variable to AAA occurrence; also to consider separately the smoking variables, expressed either as current smoker versus never smoker and ex-smoker versus never smoker, or as cigarettes/d for current smokers, without and with ex-smoker versus never smoker in the model. Deliberately, 2 highly correlated variables (eg, systolic and diastolic pressure) were not included in any of the multivariate models given the well-known distortions of coefficients their inclusion can produce. The several multivariate models also served to evaluate robustness of risk factor-AAA relationships. Significance levels were calculated for 2-tailed tests.
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Results |
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Baseline Characteristics
For all persons, mean age at screening was 50.5 years (Table 1). Mean serum cholesterol was above optimal for men and women, 8 mg/dL higher for women than men. For men and women, mean SBP and DBP were above optimal. Only 5% of men and 11% of women had optimal SBP/DBP (
120/80 and no antihypertensive drug use); the majority had hypertensive levels. About 18% of men and women had an ECG abnormality.
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Frequency of Aortic Aneurysm by Type, Data Source, and Gender
During an average follow-up of 30 years, aortic aneurysms were reported for 420 of the 10 574 men and 171 of the 8700 women (Table 2). AAA was the most common aneurysm found, accounting for a majority of cases—309 men and 109 women. Most individuals with AAA—265 men and 95 women—were identified from Medicare records only. AAA was the underlying cause of death for only 29 men and 13 women; multiple-cause coding of death certificates was the sole means of case identification for only 25 men and 8 women.
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Frequency of Coexisting Morbidity
For men and women with AAA, comorbid diseases were commonly identified during follow-up, in a significantly higher proportion than for those without AAA (Table 3). This was consistently the finding for the other cardiovascular diseases, eg, 66% of men and 71% of women with AAA had CHD diagnoses, compared with 40% of men and 30% of women without AAA. Also, chronic obstructive pulmonary disease was reported more commonly in men and women with than without AAA.
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Relationship of Single CVD Risk Factors Considered Separately to AAA
For 3 continuous major risk factors considered separately (DBP, serum cholesterol, cigarette smoking), findings with the Schoenfeld residuals method were consistent with the proportional hazards assumption of Cox analyses; exceptions were SBP and pulse pressure.
Age was strongly associated with occurrence of AAA: for persons older by 5 years at baseline, hazard ratio was 1.50 for men and 1.62 for women (Table 4). In categoric analyses, rate per 10 000 person-years was nearly 5-fold higher for men ages 60 to 64 than for men ages 40 to 44 at baseline, and over 7-fold greater for older women compared with younger women (tabular data not shown). Age-adjusted relative risk for men compared with women was 3.05 (P<0.001).
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A history of antihypertensive drug treatment in middle age was significantly related to risk of AAA in older age for men, women, and both genders combined—hazard ratios (HRs) 1.56, 1.91, and 1.69 (Table 4). For DBP, SBP, and across the JNC-VI BP strata, there was for men and for the 2 genders combined a significant gradient of risk of AAA. For pulse pressure, findings were qualitatively similar but quantitatively weaker (t value 1.82 for men, 1.64 for all). Although there was for women no significant relationship of these 4 BP variables to AAA risk, tests for gender/BP interaction were nonsignificant.
For men and women, current smoking at baseline was strongly related to occurrence of AAA, with HRs significantly larger for women than men (3.57 and 2.26 for 20 cigarettes/d versus none) (Table 4). In categoric analyses, HRs were large for current smokers of 1 to 20 cigarettes/d (3.92 for men and 3.91 for women) and for those smoking >20/d (5.74 and 5.39) compared with never smokers (tabular data not shown). For men and the 2 genders combined, former smokers were also at significantly greater risk of AAA (HRs 2.49 and 2.09); test for gender/variable interaction was nonsignificant.
Serum cholesterol at baseline was positively related to risk of AAA in older age for both men and women, HR 1.39 (P<0.001) and 1.22 (P<0.02) for 40 mg/dL higher level (about 1 SD higher) (Table 4). In categoric analyses, for men and women with serum cholesterol 240 mg/dL, compared with those <200 mg/dL, HRs were 2.56 and 1.46 (tabular data not shown).
Risk of AAA was greater with taller stature and greater weight for men and for both genders combined, with no significant gender/variable interaction (Table 4). However, overweight, as measured by body mass index (BMI), was not significantly related to AAA risk.
For persons without a diagnosis of diabetes at baseline, 1-hour post-load plasma glucose was significantly related to AAA for men and borderline significantly related for the 2 genders combined, with no significant gender/variable interaction (Table 4). For women with a history of diabetes, there was a significant association with AAA—HR 2.02 (Table 4). However, the association was nonsignificantly inverse for men and for the 2 genders combined, and there was significant evidence for gender/diabetes interaction.
Major ECG abnormalities related significantly to AAA for men and for the 2 genders combined, with no significant evidence of gender/variable interaction (Table 4).
African-American women were at greater AAA risk than other women (HR 2.09), but African-American men were at lesser AAA risk than other men, and the test for gender/race interaction was significant (Table 4).
Relationship of Risk Factors to AAA, Multivariate Analyses
Because most univariate analyses on relationships of major risk factors to AAA showed no significant gender/variable interactions (Table 4), data on men and women were combined in multivariate Cox analyses, with inclusion of gender as an independent variable (Table 5). Findings were consistent across the 5 final Cox models: each blood pressure variable, serum cholesterol, smoking, age, height, and male gender were independently and significantly related to AAA. HRs for serum cholesterol about 1 SD higher (40 mg/dL) were in the range 1.30 to 1.34 (P<0.001); for SBP about 1 SD higher (20 mm Hg), 1.10 (P<0.05); for DBP 1 SD higher (12 mm Hg), 1.12 to 1.14 (P<0.05). A history of drug treatment for hypertension was associated with 87% greater AAA risk. For current smokers overall, use of 20 cigarettes per day was associated with a risk increase of 2.4 to 2.7 times; in categoric models, for current smokers compared with never smokers HR was 5.18; for ex-smokers compared with never smokers HR was 1.41 to 2.01. Risk of AAA was from 2.0 to 2.1 times greater for men than women; 1.64 to 1.67 times greater with age older by 5 years; and 1.17 to 1.19 times greater with height greater by 7 cm (2.8 inches).
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Discussion |
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The main finding of this population-based 30-year prospective study was that the major risk factors of middle-aged men and women—serum cholesterol, blood pressure, history of antihypertensive drug treatment, cigarette smoking—were positively and independently associated with risk for abdominal aortic aneurysm in older age. Major CVD risk factors have been investigated for associations with AAA in many clinical samples. This study is one of the few with population-based long-term data; its cohort is the largest with the longest follow-up yet reported on AAA. Because of its large sample size and comparatively large number of cases, it was possible to focus on the most common diagnostic group among the aortic aneurysms, ie, abdominal aortic aneurysm, and have adequate statistical power.
Our findings are generally consistent with those reported from other prospective studies. For example, of 7682 men in the Honolulu Heart Program cohort, 138 developed AAA during 20-year follow up (among 174 aortic aneurysm cases of all types). Hypertension, high serum cholesterol, taller stature, and cigarette smoking were associated with greater risk of any aneurysm, but not glycemia or overweight.19 In the Honolulu sample, as in ours, there were few deaths attributed to aneurysm; most, 132 of 174 total cases, were identified from surgical reports.
In the Whitehall cohort, 18 403 men were followed for 18 years. In a nested case-control study of 99 men with fatal aneurysm, including 44 with AAA, mortality was significantly associated with cigarette smoking and diastolic BP, but not with glucose, height, BMI, or cholesterol. Other cardiovascular diseases, including angina and claudication at baseline, were not related to risk of fatal aneurysm.18
Comparatively short follow-up data are available from 3 other studies.1,15–17 The American Cancer Society study of 800 000 volunteers identified 519 cases (431 men and 88 women) and reported that hypertension and smoking were more frequently found among decedents from any aortic aneurysm at 6-year follow-up.17 In the Edinburgh Artery Study of peripheral vascular disease, 1592 men and women were screened at ages 55 to 74 by ultrasound; 34 cases of AAA were so identified and 6 more were clinically known. Based on a case-control analysis, with major CVD risk factors assessed 5 years earlier, only cigarette smoking was significantly associated with AAA. Persons with AAA had more clinical and subclinical markers of systemic vascular diseases, including peripheral arterial disease, reduced ankle-brachial index (ABI), and angina than did controls.16 In the Cardiovascular Health Study (CHS), ultrasound screening identified 471 people with AAA among 4741 men and women ages 65 to 90 years who had been screened for baseline risk factors 1 to 4 years earlier. Significant associations were found of AAA with age, male gender, smoking, height, weight, treatment for hypertension, low-density lipoprotein cholesterol, and inversely with high-density lipoprotein cholesterol. Clinical CHD (angina, myocardial infarction) and subclinical CVD (decreased ABI, carotid stenosis, and carotid intimal medial thickening) were more common among AAA cases. Neither glycemia nor blood pressure was significantly associated with AAA.15 During 5-year follow-up, CHS participants with AAA were at higher risk for new CVD events, CVD death, and total mortality than persons with baseline CVD diagnoses other than AAA.1 This suggested to the authors that small AAA, rarely fatal in themselves, were markers for severity of underlying cardiovascular disease.1
Data from large cross-sectional studies are consistent with the prospective data, supporting associations of AAA with male gender, age, cigarette smoking, serum cholesterol, and coexisting cardiovascular diseases.3,11,31 A study of over 75 000 veterans ages 50 to 79 years identified 1031 AAA by ultrasound and reported associations with stature, serum cholesterol, and hypertension. A family history of aneurysm, reported by 5% of these veterans, was associated with a nearly 2-fold greater odds ratio. Diabetes and African-American race were inversely associated with prevalent AAA.3 Other cross-sectional studies also found inverse or no associations of AAA with diabetes and glycemia4,9,32 or with African-American race.3,4 Thus, neither prospective nor cross-sectional studies strongly support an association of diabetes and AAA, in contrast to studies showing diabetes to be a risk factor for other CVD, including coronary and peripheral arterial disease and stroke. This may represent type I error and/or the impact of competing CVD mortality among diabetics. Also, the deleterious effect of diabetes on medium and small arteries may be clinically unimportant for AAA given the large caliber of the aorta.
As to major, minor, and total ECG abnormalities at baseline, generally regarded as indicative of subclinical CVD and present in 18% of CHA participants at baseline, only major ECG abnormalities in men and in the 2 genders combined related significantly to AAA in univariate analyses, but not in multivariate analyses. On the other hand, the 30-year follow-up data show an association of AAA with CHD, stroke, and PVD, as well as COPD. Other studies, including the CHS, have reported a higher likelihood of other CVD among aneurysm patients.1,6,8,31 Studies of children and young adults found associations of aortic (as well as coronary) plaque with lipid and glucose abnormalities, hypertension, and smoking.33–36 It is not known whether such aortic lesions observed in youth are precursors of adult aneurysms.
A limitation of the present study is that Medicare records and search of death certificates were used to identify clinical AAA cases. An aneurysm so detected could have been symptomatic, ie, the reason for the medical encounter, or a finding during medical evaluation of other conditions, eg, a CT scan for abdominal pain. Period prevalence of AAA for the CHA cohort of 0.9% based on medical records seems low when compared with rates of up to 5% reported in community sample surveys5,9,10,11,37,38 and over 10% for CHS participants.15 Differences in prevalence across these studies are probably due at least in part to variation in measurement methods and definition of aortic dilation. Thus, one limitation of our study is ascertainment bias, ie, missing of cases. Also, the association of AAA with other comorbidity may be exaggerated, in that sick older people are likely to undergo more diagnostic procedures than well older people and are therefore more likely to have any clinically silent disease detected. Another source of ascertainment bias was baseline age, because older people had longer follow-up in the Medicare database. The Cox method corrects for this bias at least in part by using person-years of observation as the basis for calculating rates.
Aneurysm mortality was low in the CHA cohort, and most cases were identified from Medicare records. Studies relying only on mortality will substantially underestimate occurrence of AAA.19 Our Medicare cases probably represent a mixture of clinically significant and small aneurysms. It is difficult, given the coding procedure, to distinguish them. We have no data on nonfatal aneurysms before age 65 unless the diagnosis was carried forward into Medicare records of survivors. However, the cases we analyzed likely reflect the spectrum of clinically detected disease in the Medicare age group.
Medicare data are a reasonably unbiased source of cases because about 96% of eligible men and women ages 65 and older participate in Medicare.39 Only the records for 1984–2000 were available to us; lifetime occurrence of AAA and of other CVD are bound to be higher with longer follow-up.
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Conclusions |
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The 30-year prospective CHA data demonstrate strong associations of major CVD risk factors measured in middle age to diagnosis of clinical AAA in older age. Our findings are generally consistent with those from other population studies. Other CVD comorbidity was common among AAA cases. These data add further support to the concept that prevention of AAA morbidity and mortality may be possible through population prevention and control of known major CVD risk factors.
Perspectives
Extensive data are now available demonstrating that, for both women and men, favorable levels of all major risk factors in young adulthood and middle age—serum total cholesterol <200 mg/dL, SBP/DBP 120/80 mm Hg, no current smoking, and no history of diabetes or heart attack—lead to low rates (endemic, not epidemic) of CHD, stroke, and all CVD in older age, as well as sizably increased longevity.40 It is a reasonable inference from the findings of the present study that such people at low CHD-CVD risk are also at low risk for clinical abdominal aortic aneurysm. At present, a small minority of young adult and middle-aged men and women are at such low risk. Appropriately then, current strategic priorities for CHD-CVD prevention emphasize efforts by medical care and public health to increase the proportions of low-risk individuals throughout the population. The data here suggest that success in these efforts will also markedly reduce abdominal aortic aneurysm as a major clinical problem for older people. This is yet another important reason to underscore the importance of preventing and controlling all the major risk factors.
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Acknowledgments |
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This research was supported by grants from the American Heart Association and its Chicago and Illinois affiliates, the Illinois Regional Medical Program, the National Heart, Lung, and Blood Institute (HL21010 and HL03387), the Chicago Health Research Foundation, and private donors. We are indebted to the officers and employees of the Chicago companies and organizations whose cooperation and assistance made this study possible, to the staff members and volunteers involved in the Chicago Heart Association Detection Project in Industry, and to our departmental colleagues. An extensive list of colleagues who contributed to this endeavor is given in Cardiology. 1993;82:191–222.
Received July 23, 2002; first decision August 27, 2002; accepted May 16, 2003.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
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- Newman AB, Arnold AM, Burke GL, O’Leary DH, Manolio TA. Cardiovascular disease and mortality in older adults with small abdominal aortic aneurysms detected by ultrasonography: the Cardiovascular Health Study. Ann Intern Med. 2001; 134: 182–190.
[Abstract/Free Full Text] - Gillum RF. Epidemiology of aortic aneurysm in the United States. J Clin Epidemiol. 1995; 48: 1289–1298.[CrossRef][Medline] [Order article via Infotrieve]
- Lederle FA, Johnson GR, Wilson SE, Chute EP, Littooy FN, Bandy KD, Drupski WC. Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group. Ann Intern Med. 1997; 126: 441–449.
[Abstract/Free Full Text] - LaMorte WW, Scott TE, Menzoian JO. Relationship of cardiovascular risk factors to racial differences in femoral bypass surgery and abdominal aortic aneurysmectomy in Massachusetts. J Vasc Surg. 1995; 21: 422–431.[CrossRef][Medline] [Order article via Infotrieve]
- Collin J, Walton J, Araujo L, Lindsell D. Oxford screening programme for abdominal aortic aneurysms in men aged 65 to 74 years. Lancet. 1988; 2: 613–615.[Medline] [Order article via Infotrieve]
- MacSweeney ST, O’Meara M, Alexander C, O’Malley MK, Powell JT, Greenhalgh RM. High prevalence of unsuspected abdominal aortic aneurysms in patients with confirmed symptomatic peripheral or cerebral arterial disease. Br J Surg. 1993; 80: 582–584.[Medline] [Order article via Infotrieve]
- Powell JT, Worrell P, MacSweeney ST, Franks PJ, Greenhalgh RM. Smoking as risk factor for abdominal aortic aneurysm. Ann NY Acad Sci. 1996; 800: 246–248.[CrossRef][Medline] [Order article via Infotrieve]
- Blanchard AF, Armenian HK, Friesen PP. Risk factors for abdominal aortic aneurysm: results of a case-control study. Am J Epidemiol. 2000; 151: 575–583.
[Abstract/Free Full Text] - Bengtsson H, Bergqvist D, Ekberg O, Janzon L. A population-based screening of abdominal aortic aneurysms (AAA). Eur J Vasc Surg. 1991; 5: 53–57.[CrossRef][Medline] [Order article via Infotrieve]
- Simoni G, Gianotti A, Ardia A, Baiardi Galleano R, Civalleri D. Screening study of abdominal aortic aneurysm in a general population: lipid parameters. Cardiovasc Surg. 1996; 4: 445–448.[CrossRef][Medline] [Order article via Infotrieve]
- Pleumeekers HJ, Hoes AW, van der Does E, van Urk H, Hofman A, de Jong PT, Grobbee DE. Aneurysms of the abdominal aorta in older adults. The Rotterdam Study. Am J Epidemiol. 1995; 142: 1291–1299.
[Abstract/Free Full Text] - Naydeck BL, Sutton-Tyrrell K, Schiller KD, Newman AB, Kuller LH. Prevalence and risk factors for abdominal aortic aneurysms in older adults with and without isolated systolic hypertension. Am J Cardiol. 1999; 83: 759–764.[CrossRef][Medline] [Order article via Infotrieve]
- Sutton-Tyrrell K, Newman AB, Simonsick EM, Havlik R, Pahor M, Lakatta E, Spurgeon H, Vaitkevicius P. Aortic stiffness is associated with visceral adiposity in older adults enrolled in the study of health, aging, and body composition. Hypertension. 2001; 38: 429–433.
[Abstract/Free Full Text] - Johnson G Jr, Avery A, McDougal EG, Burnham SJ, Keagy BA. Aneurysms of the abdominal aorta. Incidence in blacks and whites in North Carolina. Arch Surg. 1985; 120: 1138–1140.[Abstract]
- Alcorn HG, Wolfson SK, Jr, Sutton-Tyrell K, Kuller LH, O’Leary D. Risk factors for abdominal aortic aneurysms in older adults enrolled in the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol. 1996; 16: 963–970.
[Abstract/Free Full Text] - Lee AJ, Fowkes FG, Carson MN, Leng GC, Allan PL. Smoking, atherosclerosis and risk of abdominal aortic aneurysm. Eur Heart J. 1997; 18: 671–676.
[Abstract/Free Full Text] - Hammond EC, Garfinkel L. Coronary heart disease, stroke, and aortic aneurysm. Arch Environ Health. 1969; 19: 167–182.
- Strachan DR. Predictors of death from aortic aneurysms among middle-aged men: the Whitehall study. Br J Surg. 1991; 78: 401–404.[Medline] [Order article via Infotrieve]
- Reed D, Reed C, Stemmermann G, Hayashi T. Are aortic aneurysms caused by atherosclerosis? Circulation. 1992; 85: 205–211.
[Abstract/Free Full Text] - Pooling Project Research Group. Relationship of blood pressure, serum cholesterol, smoking habit, relative weight, and ECG abnormalities to incidence of major coronary events: final report of the Pooling Project. J Chronic Dis. 1978; 31: 201–306.[CrossRef][Medline] [Order article via Infotrieve]
- Stamler J, Dyer AR, Shekelle RB, Neaton J, Stamler R. Relationship of baseline major risk factors to coronary and all cause mortality and to longevity: findings from the long-term follow-up of Chicago cohorts. Cardiology. 1993; 82: 191–222.[Medline] [Order article via Infotrieve]
- Orencia AJ, Daviglus ML, Dyer AR, Walsh M, Greenland P, Stamler J. One-hour postload plasma glucose and risks of fatal coronary heart disease and stroke among nondiabetic men and women: the Chicago Heart Association Detection Project in Industry (CHA) Study. J Clin Epidemiol. 1997; 50: 1369–1376.[CrossRef][Medline] [Order article via Infotrieve]
- National Center for Health Statistics. International Classification of Diseases, Adapted for Use in the United States. 8th rev. Washington, DC: US Department of Health and Human Services, Public Health Service; 1967;PHS 1693.
- Department of Health and Human Services. International Classification of Diseases. 9th rev. Clinical Modification. Washington, DC: US Department of Health and Human Services, Public Health Service; 1980;PHS 80-1260.
- World Health Organization. International Classification of Diseases and Related Health Problems. 10th rev. Geneva, Switzerland: World Health Organization; 1992.
- National Center for Health Statistics. National Death Index Users Manual. Hyattsville, MD: US Department of Health and Human Services, Public Health Service; 2000.
- Sonesson B, Hansen F, Lanne T. Abdominal aortic aneurysm: a general defect in the vasculature with focal manifestations in the abdominal aorta? J Vasc Surg. 1997; 26: 247–254.[CrossRef][Medline] [Order article via Infotrieve]
- The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1997; 157: 1413–2446.[Abstract]
- Cox DR. Regression models and life-tables. JR Stat Soc (B). 1972; 34: 187–202.
- Therneau TM, Grambsch PM, Fleming TR. Martingale-based residuals for survival models. Biometrika. 1990; 771: 147–160.[CrossRef]
- Allardice JT, Allwright GJ, Wafula JMC, Wyatt AP. High prevalence of abdominal aortic aneurysm in men with peripheral vascular disease: screening by ultrasonography. Br J Surg. 1988; 75: 240–242.[Medline] [Order article via Infotrieve]
- Mattes E, Davis TM, Yang D, Ridley D, Lund H, Norman PE. Prevalence of abdominal aortic aneurysms in men with diabetes. Med J Aust. 1997; 166: 630–633.[Medline] [Order article via Infotrieve]
- McGill HC, Jr, McMahan CA, Malcolm GT, Oalmann MC, Strong JP. Relation of glycohemoglobin and adiposity to atherosclerosis in youth. Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Arterioscler Thromb Vasc Biol. 1995; 15: 431–440.
[Abstract/Free Full Text] - McGill HC, Jr, Strong JP, Tracy RE, McMahan CA, Oalmann MC. Relation of a postmortem renal index of hypertension to atherosclerosis in youth. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Arterioscler Thromb Vasc Biol. 1995; 15: 2222–2228.
[Abstract/Free Full Text] - McGill HC Jr, McMahan CA, Malcolm GT, Oalmann MC, Strong JP. Effects of serum lipoproteins and smoking on atherosclerosis in young men and women. The PDAY Research Group. Pathobiological Determinants of Atherosclerosis in Youth. Arterioscler Thromb Vasc Biol. 1997; 17: 95–106.
[Abstract/Free Full Text] - Berenson GS, Srinivasan SR, Bao W, Newman WP III, Tracy RE, Wattingney WA. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. The Bogalusa Heart Study. N Engl J Med. 1998; 338: 1650–1656.
[Abstract/Free Full Text] - Bickerstaff LK, Hollier LH, Van Peenen HJ, Melton LJ III, Pairolero PC, Cherry KJ. Abdominal aortic aneurysms: the changing natural history. J Vasc Surg. 1984; 1: 6–12.[CrossRef][Medline] [Order article via Infotrieve]
- The Multicentre Aneurysm Screening Study Group. The Multicentre Aneurysm Screening Study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomized controlled trial. Lancet. 2002; 360: 1531–1539.[CrossRef][Medline] [Order article via Infotrieve]
- National Center for Health Statistics. Access to Health Care. Part 3. Older Adults. Washington, DC: Department of Health and Human Services; 1997: 3.PHS 97-1526.
- Stamler J, Stamler R, Neaton JD, Wentworth D, Daviglus ML, Garside D, Dyer AR, Greenland P, Liu K. Low risk factor profile and long-term cardiovascular and non-cardiovascular mortality and life expectancy: findings for 5 large cohorts of young adult and middle-aged men and women. JAMA. 1999; 282: 2012–2018.
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